Liver disease may be detected during a physical examination. During part of the exam, the doctor will lightly tap your abdomen above the liver (percussion). The resulting sound may indicate a change in the size or position of the liver.

Liver health can also be determined by gently pressing over the right upper part of the abdomen.

Further evaluation can involve blood tests looking for elevations of liver enzymes (see next page).

9THE LIVER

Enzymes (proteins) from the liver are normally found in the blood as a result of normal aging and degeneration of liver cells (called LFTS liver function tests)

ALT

Almandine aminotransferase

AST

Aspartate aminotransferase

GGTP

Gamma -glutamyltransferase

10THE LIVER

Liver enzymes (LFTs)

6 of all patients have elevated enzymes. The most common causes are

Alcohol use

Obesity

Hepatitis C

11HEPATITIS

INFLAMMATION OF THE LIVER

CAUSED BY

VIRUSES - HEPATITIS A, B, C, D, E, G

OTHER INFECTIONS (MONONUCLEOSIS)

CHEMICALS

ALCOHOL

ACETAMINOPHEN

12HEPATITIS

A virus is much smaller than a human cell and much simpler. It is a string of genes (DNA or RNA) covered by a coat of protein. The virus cannot accomplish all the complex functions that normal cells can and in fact can really only reproduce using the human cell as a host. (When a virus invades a cell, it can use the cells own mechanisms to reproduce) The hepatitis virus invades the liver cell and ultimately, using it to reproduce, causes damage (release of liver enzymes) and death of the liver cell.

Acute hepatitis is where the disease develops quickly, has symptoms and lasts less than 6 months.

Chronic hepatitis is where the symptoms and disease last longer than 6 months.

ACUTE HEPATITIS CAN RESOLVE TOTALLY OR GO ON TO A CHRONIC STAGE

15 VIRAL HEPATITIS

VIRAL HEPATITIS TYPES

A

CALLED INFECTIOUS HEPATITIS (HAV)

B

CALLED SERUM HEPATITIS (HBV)

C

PREVIOUSLY CALLED NON - A NON - B, NOW HCV

D

DEFECTIVE RNA VIRUS

NEEDS B TO INFECT

E

LIKE A, ORAL/FECAL TRANSMITTED

16HEPATITIS A (HAV)

Hepatitis A is caused by infection with the hepatitis A virus, which is an RNA virus in the picornavirus family.

Only one virus has been discovered, unlike some other viruses that have subtypes.

This type of hepatitis is vaccine preventable

SourceCenter for Disease Control

17HEPATITIS A (HAV)

Hepatitis A is responsible for about 20,000 to 40,0000 infections a year in the United States. While most are associated with symptoms, death is rarely associated with this type of hepatitis (due to fulminant hepatitis liver failure)

18WORLDWIDE HEPATITIS A PREVALENCE (CDC) 19HEPATITIS A (HAV)

Clinical Features

Incubation period is usually about 30 days after exposure, the range is 15 50 days

Jaundice (turning yellow) is most commonly seen in the older patients

Under 6 years old (10)

6 to 14 years old (40 50)

Greater than 14 years old (70 80)

Fatigue

Dark urine

Fever

Nausea and vomiting

Abdominal pain

Complications of this type of viral infection include rare liver failure and relapsing hepatitis

Chronic sequelae are not seen

33 of the US population has evidence of past infection and thus immunity

20HEPATITIS A (HAV)

Diagnosis - Hepatitis Panel

For diagnosis of Hepatitis A -IgM anti-HAV

Liver Enzymes

21EVENTS IN HEPATITIS A INFECTION (CDC)

As the immune system responds to the infection, the amount of virus in the blood (viremia) and in the stool (HAV in stool) disappears. The liver enzyme, ALT goes up at the beginning of the infection, but descreases to normal at about 8 weeks. IgM shows acute infection and IgG is positive long term.

22HEPATITIS A (HAV)

HAV Transmission

Close personal contact

Household member

Sex contact

Childcare centers

Contaminated food or water

Fecal oral contact

Contaminated shellfish

Infected food handlers

Blood exposure

rare

23HEPATITIS A (HAV)

HAV Treatment

No specific medical treatment

Avoid alcohol and all medications that are metabolized in the liver

Manage symptoms

If the spleen is enlarged avoid activities that could lead to abdominal pressure or injury

24HEPATITIS A (HAV)

HAV Prevention

Wash hands

Use gloves when appropriate

Risk reduction if involved in oral/anal sexual practices

Risk reduction if involved in intravenous drug use

Vaccination

25HEPATITIS A (HAV)

HAV Prevention (continued)

Vaccination

Pre-exposure Vaccination

Persons at increased risk for infection

Travelers to intermediate and high HAV-endemic countries

Homosexual and bisexual men (men who have sex with men)

Persons with HIV/AIDS

Drug users

Persons with chronic liver disease including Hepatitis C

Persons with a diagnosis of clotting factor disorder

Persons with occupational risks

Communities with high rates of hepatitis A e.g., Alaska Natives, American Indians

Only plasma tested negative for hepatitis B, HIV, and antibodies to hepatitis C are used

Provides protection against hepatitis A through passive transfer of antibody

When administered within 2 weeks after an exposure to hepatitis A virus, IG is 80 90 effective in preventing hepatitis A

27HEPATITIS A (HAV)

HAV Vaccines first licensed in 1995

Vaccines are virus vaccines where the virus has been inactivated

Both vaccines are highly immunogenic where 100 of those vaccinated with 2 doses will seroconvert to a protected level

New recommendations in 2005 are for routine vaccination of all children in the US beginning at 1 year of age

HAVRIX

The standard primary course of vaccination with HAVRIX consists of two doses, the first administered at the elected date and the second one month later. If necessary, the second dose may be administered a minimum of two weeks following the first dose. A booster is recommended at any time between 6 and 12 months after the initiation of the primary course in order to ensure long term antibody titers. In the event a subject is expected to be exposed to a high risk of contracting hepatitis A before the completion of the primary immunization scheme, concomitant administration of HAVRIX ISG might be considered.

HAVRIX is indicated for active immunization of persons 2 years of age against disease caused by hepatitis A virus (HAV). HAVRIX will not prevent hepatitis caused by other agents such as hepatitis B virus, hepatitis C virus, hepatitis E virus, or other pathogens known to infect the liver.

There is also a combined HAV and HBV vaccine available TWINRIX which offers the added advantage of providing protection against two viral hepatitis infections.

Source GlaxoSmithKline Pharmaceuticals.

28HEPATITIS A (HAV)

HAV Vaccines

VAQTA is indicated for active pre-exposure prophylaxis against disease caused by hepatitis A virus in persons 2 years of age and older.

VAQTA is for intramuscular injection. A booster dose of VAQTA may be given at 6 to 12 months following the initial dose of other inactivated hepatitis A vaccines (e.g., HAVRIX).

Primary immunization should be given at least 2 weeks prior to expected exposure to HAV.

Source Merck Co., Inc

29HEPATITIS B (HBV)

Hepatitis B is a DNA virus of the class of viruses known as hepadnaviridae.

The Hepatitis B virus is 100 times more infectious than the HIV virus.

Hepatitis B is vaccine preventable.

Source Center for Disease Control

30HEPATITIS B (HBV)

Hepatitis B virus is composed of several different parts

Hepatitis B Surface Antigen

Outer surface membrane

Primary component of Hepatitis B vaccines

This structure causes the production of a protective, neutralizing antibody that provides long - term protection from the Hepatitis B virus

31HEPATITIS B (HBV)

Hepatitis B virus is composed of several different parts

The inner core contains

Hepatitis B core antigen (HBcAg)

Hepatitis B e antigen (HBeAg)

32HEPATITIS B (HBV)

Hepatitis B virus infection is seen in Americans each year

33HEPATITIS B (HBV)

Hepatitis B virus infection

Of the total number of those infected, a small percentage die from cirrhosis (top picture) and primary liver cancer (bottom picture)

34HEPATITIS B (HBV)

Clinical course symptoms

Jaundice

fatigue/abdominal pain

appetite loss

nausea/vomiting

mild fever

dark urine

One third of adults 90 of children have no symptoms

Symptoms last 1-4 weeks up to 6 months

90-95 recover within 6 months with lifelong immunity

50 develop acute liver disease

35HEPATITIS B (HBV)

Clinical course 10 of adults who are infected do not clear the virus and develop what is called Chronic HBV infection.

These patients develop chronic liver disease which can be either persistently mild or aggressive. 20 25 of these patients die prematurely due to cirrhosis or liver failure.

30 50 of all infected 1 to 5 year olds and 80 90 of all infants develop chronic infection

36WHAT IS CIRRHOSIS ?

Scarring of the liver with loss of function

Liver function tests may be normal due to a decrease in the number of normal liver cells

Dont use an infected persons toothbrush, razor, or anything else that could have blood on it

48HEPATITIS B (HBV)

Prevention

Vaccination should be offered to

Persons with more than one sex partner in 6 months

Men who have sex with men (MSM)

Persons diagnosed with a sexually transmitted disease (STD)

Commercial sex workers

Illegal injectable drug users

Persons with HIV/AIDS

Persons with chronic liver disease including Hepatitis C

Inmates

Healthcare workers

Staff and clients (developmentally disabled)

Persons receiving hemodialysis

Alaskan Natives and Pacific Islanders

Adopted persons from HBV endemic countries

Recipients of certain blood products

49HEPATITIS B (HBV)

Prevention

Vaccine first licensed in 1981

Two inactivated virus vaccines available in the US

Engerix B made by GlaxoSmithKline

Recombivax HB made by Merck

Both vaccines are highly immunogenic where after 3 doses, 90 of young adults and 95 of infants, children and adolescents develop an antibody response

Immune memory lasts 15 years

Hepatitis B vaccine produces antibody response series of three injections

Give initial dose, then next one at 1 month and last one 6 months later for adults and older children, though dosing can be at 2 and 4 months after initial shot, or 1 and 4 months after initial shot (all schedules are approved)

All high risk babies should get vaccinated. Infants get their first shot within 12 hours after birth, the second shot at age 1 to 2 months and the third shot between the ages of 6 to 18 months.

Peak level achieved 7-10 months after initial dose

50HEPATITIS B (HBV)

Prevention

Twinrix is a combination hepatitis A and B vaccine made by GlaxoSmithKline and approved for persons aged 18 years and older. It is indicated for persons at risk for both hepatitis A and B

It is administered in a 3 dose series at 0, 1, and 6 months

51HEPATITIS B (HBV)

Prevention Note

If a patient does not complete the series of vaccines indicated, they should just restart where they left off. There is not need to restart from the first dose.

52HEPATITIS B (HBV)

Treatment for Hepatitis B

Alpha-interferons were the first drugs approved in the United States for the treatment of chronic hepatitis B.

Interferon treatment is recommended for individuals who have "replicative disease" (HBeAg positive).

About 40 of such individuals will lose serum HBeAg after 16 weeks of treatment with interferon-alpha.

Loss of HBeAg is correlated with an improved prognosis.

Patients with severe, decompensated liver disease (eg. encephalopathy, ascites, very high serum bilirubin, prolonged prothrombin time, etc.) should not generally be treated with interferon alfa except in the setting of an approved clinical study.

The recommended dose of interferon alfa-2b for the treatment of chronic hepatitis B is 5,000,000 units daily, administered by subcutaneous or intramuscular injection, for a total of 16 weeks. The patient must be monitored carefully during the treatment period for side effects including flu-like symptoms, depression, rashes, other reactions and abnormal blood counts.

53HEPATITIS B (HBV)

Treatment for Hepatitis B (continued)

Other treatment options for chronic hepatitis B include nucleoside analogues

Lamivudine , also known as 3TC and is also effective against HIV.

Lamivudine is taken orally at 100 mg/day for chronic hepatitis B.

In studies where they were compared, lamivudine was equally effective to interferon-alpha in inducing a loss of serum HBeAg. It also has been shown to improve liver biopsy results.

Adevofir dipivoxil

The dose is 10 mg/day for chronic hepatitis B.

At the present time, other nucleoside analogues are being studied in clinical trials. The combination of interferon-alpha and a nucleodide analogue, two nucleoside analogues together (such as lamivudine and adefovir) are also under investigation.

54HEPATITIS D (HDV)

HDV is a defective single-stranded RNA virus that requires the helper function of HBV to replicate. HDV requires HBV for synthesis of envelope protein composed of HBsAg, which is used to encapsulate the HDV viral nucleic acid.

Source Center for Disease Control

55(No Transcript) 56HEPATITIS D (HDV)

Clinical

HDV infection can be acquired either as a co-infection with HBV or as a superinfection of persons with chronic HBV infection.

Persons with HBV-HDV co-infection may have more severe acute disease and a higher risk of fulminant hepatitis (2-20) compared with those infected with HBV alone

Chronic HBV infection appears to occur less frequently in persons with HBV-HDV co-infection.

In long-term studies of chronic HBV carriers with HDV superinfection, 70-80 have developed evidence of chronic liver diseases with cirrhosis compared with 15-30 of patients with chronic HBV infection alone

58

In most persons with HBV-HDV co-infection, both IgM antibody to HDV (anti-HDV) and IgG anti-HDV are detectable during the course of infection.

However, in about 15 of patients the only evidence of HDV infection may be the detection of either IgM anti-HDV alone during the early acute period of illness or IgG anti-HDV alone during convalescence.

Anti-HDV generally declines to sub-detectable levels after the infection resolves and there is no serologic marker that persists to indicate that the patient was ever infected with HDV.

59

Hepatitis Delta Antigen (HDAg) can be detected in serum in only about 25 of patients with HBV-HDV co-infection. When HDAg is detectable it generally disappears as HBsAg disappears and most patients do not develop chronic infection.

Tests for IgG anti-HDV are commercially available in the United States.

60

In patients with chronic HBV infection who are super-infected with HDV several characteristic serologic features generally occur, including

the titer of HBsAg declines at the time HDAg appears in the serum

HDAg and HDV RNA remain detectable in the serum because chronic HDV infection generally occurs in most patients with HDV superinfection, unlike the case with co-infection

high titers of both IgM and IgG anti-HDV are detectable, which persist indefinitely.

61HEPATITIS D (HDV)

Transmission

The modes of HDV transmission are similar to those for HBV, with percutaneous exposures the most efficient (blood from an infected person enters the body of a person who is not immune).Sexual transmission of HDV is less efficient than for HBV. Perinatal HDV transmission is rare.

62HEPATITIS D (HDV)

Transmission

Risk groups include

Injection drug users

Men who have sex with men

Hemodialysis patients

Sex contacts of infected persons

Healthcare and public safety officers

Infants born to infected mothers (very rare)

63HEPATITIS D (HDV)

Prevention

Because HDV is dependent on HBV for replication, HBV-HDV co-infection can be prevented with either pre- or postexposure prophylaxis for HBV.

Virus excretion in stools occurred approximately 4 weeks after oral ingestion and persisted for about 2 weeks.

Both IgM and IgG antibody to HEV (anti-HEV) are elicited following HEV infection.

The titer of IgM anti-HEV declines rapidly during early convalescence.

IgG anti-HEV persists and appears to provide at least short-term protection against disease.

69

No serologic tests to diagnose HEV infection are commercially available in the United States.

70HEPATITIS E (HEV)

Clinical Features

The period of infectivity following acute infection has not been determined but virus excretion in stools has been demonstrated up to 14 days after illness onset.

In most hepatitis E outbreaks, the highest rates of clinically evident disease have been in young to middle-age adults

No evidence of chronic infection has been detected in long-term follow-up of patients with hepatitis E.

71HEPATITIS E (HEV)

Clinical Features

Case-fatality rate Overall, 1-3 Pregnant women, 15-25

Illness severity is increased with age

Chronic sequelae None identified

72HEPATITIS E (HEV)

Transmission

HEV is transmitted primarily by the fecal-oral route and fecally contaminated drinking water is the most commonly documented vehicle of transmission.

Although hepatitis E is most commonly recognized to occur in large outbreaks, HEV infection accounts for 50 of acute sporadic hepatitis in both children and adults in some high endemic areas.

Risk factors for infection among persons with sporadic cases of hepatitis E have not been defined.

Unlike hepatitis A virus, which is also transmitted by the fecal-oral route, person-to-person transmission of HEV appears to be uncommon. However, nosocomial transmission, presumably by person-to-person contact, has been reported to occur. Virtually all cases of acute hepatitis E in the United States have been reported among travelers returning from high HEV-endemic areas.

73HEPATITIS E (HEV)

Diagnosis

No serologic tests to diagnose HEV infection are commercially available in the United States.

74HEPATITIS E (HEV)

Prevention

Prevention of hepatitis E relies primarily on the provision of clean water supplies.

Prudent hygienic practices that may prevent hepatitis E and other enterically transmitted diseases among travelers to developing countries include avoiding

drinking water (and beverages with ice) of unknown purity

uncooked shellfish

uncooked fruits or vegetables that are not peeled or prepared by the traveler

No products are available to prevent hepatitis E.

75HEPATITIS E (HEV)

Treatment

Supportive

No medications are available

Treat symptoms with PRN (as needed) medications

76HEPATITIS G (HGV)

Hepatitis G is a newly discovered form of liver inflammation caused by hepatitis G virus (HGV), a distant relative of the hepatitis C virus.

HGV, also called hepatitis GB virus, was first described early in 1996.

HGV is a positive-strand RNA virus belonging to the family Flaviviridae.

Little is known about the frequency of HGV infection, the nature of the illness, or how to prevent it. What is known is that transfused blood containing HGV has caused some cases of hepatitis.

77HEPATITIS G (HGV)

HGV has been identified in between 1-2 of blood donors in the United States.

Often patients with hepatitis G are infected at the same time by the hepatitis B or C virus, or both.

In about three of every thousand patients with acute viral hepatitis, HGV is the only virus present.

The virus has been identified in as many as 20 of patients with long-lasting viral hepatitis, some of whom also have hepatitis C.

78HEPATITIS G (HGV)

Clinical

Some researchers believe that there may be a group of GB viruses, rather than just one. Others remain doubtful that HGV actually causes illness. If it does, the type of acute or chronic (long-lasting) illness that results is not clear.

Diagnosis is made by confirming the presence of HGV in the blood by detecting HGV-RNA.

When diagnosed, acute HGV infection has usually been mild and brief.

There is no evidence of serious complications, but it is possible that, like other hepatitis viruses, HGV can cause severe liver damage resulting in liver failure.

79HEPATITIS G (HGV)

Transmission

Transfused blood containing HGV has caused some cases of hepatitis. For this reason, patients with hemophilia and other bleeding conditions who require large amounts of blood or blood products are at risk of hepatitis G.

HGV has been identified in between 1-2 of blood donors in the United States.

Also at risk are

Patients with kidney disease who undergo hemodialysis

Injection drug users

It is possible that an infected mother can pass on the virus to her newborn infant

Sexual transmission also is a possibility

80HEPATITIS G (HGV)

Treatment

There is no specific treatment for any form of acute hepatitis. Patients should rest in bed as needed, avoid alcohol, and be sure to eat a balanced diet.

Prognosis

What little is known about the course of hepatitis G suggests that illness is mild and does not last long.

Prevention

Since hepatitis G is a blood-borne infection, prevention relies on avoiding any possible contact with contaminated blood. Drug users should not share needles, syringes, or other equipment.

81SPECIAL CONSIDERATIONS

Chemically Dependence Counselors

In the typical counseling setting, it is virtually impossible to contract hepatitis

The chemical dependence patient may exhibit some symptoms early in the disease process that could mimic mild withdrawal (especially opiate withdrawal)

Remember to reinforce the facts that Hepatitis A is a self limited disease and that there are treatments available for Hepatitis B and C.

Remember to reinforce the fact that use of alcohol and other drugs is detrimental to the course of hepatitis

82SPECIAL CONSIDERATIONS

Chemically Dependent Patients

Alcohol will worsen all forms of hepatitis

Alcohol alone can cause a form of hepatitis (alcohol induced hepatitis)

More than 2 million Americans suffer from alcohol-related liver disease. Its symptoms include fever, jaundice (abnormal yellowing of the skin, eyeballs, and urine), and abdominal pain. Alcoholic hepatitis can cause death if drinking continues. If drinking stops, this condition often is reversible. About 10 to 20 percent of heavy drinkers develop alcoholic cirrhosis, or scarring of the liver.

Alcohol can also cause a condition know as fatty liver, which is sometimes misinterpreted as hepatitis. The liver enzymes are elevated and the liver is enlarged on examination. However, this is due to the body using alcohol as an energy source and the fat from the food intake being stored in the liver. The condition will resolve in several weeks once alcohol use is stopped.

83SPECIAL CONSIDERATIONS

Chemically Dependent Patients

Some medications can cause or worsen hepatitis

Naltrexone used as an opiate blocker or alcohol craving reducer

Statins used to treat hypercholesterolemia

Any drug that impacts negatively on the immune system can have a detrimental effect on the course of liver disease

A 23 year-old woman developed biochemical signs of acute severe hepatitis together with confusion and flapping tremor after snorting a large dose of cocaine. Blood levels of cocaine were very high and a liver biopsy was performed a few days later showing centrilobular necrosis. She recovered completely with conservative measures.

Cocaine toxicity should be considered in similar cases of fulminant liver failure.

The link between toxic hepatitis and exposure to organic solvents is relatively well-documented, but there are no specific laboratory or histologic findings diagnostic of chemical-induced hepatitis. Clinical history, therefore, is very important in making a diagnosis. A history of glue sniffing is sometimes overlooked and glue sniffing has not received much attention as a cause of hepatitis. Toluene, a main organic solvent in glue, is known to cause disturbances in various organs such as the heart, nervous system, liver and kidneys. We present a case of hepatitis in an individual who has sniffed glue for euphoria for 3 years.

There is an increasing tendency towards glue sniffing among young adolescents today, so toxicity caused by exposure to organic solvents should be considered as one possible cause of hepatitis in young adolescents.

BACKGROUND Sublingual buprenorphine is used as a substitution drug in heroin addicts. Although buprenorphine inhibits mitochondrial function at high concentrations in experimental animals, these effects should not occur after therapeutic sublingual doses, which give very low plasma concentrations.

CASE REPORTS We report four cases of former heroin addicts infected with hepatitis C virus and placed on substitution therapy with buprenorphine. These patients exhibited a marked increase in serum alanine amino transferase (30-, 37-, 13- and 50-times the upper limit of normal, respectively) after injecting buprenorphine intravenously and three of them also became jaundiced. Interruption of buprenorphine injections was associated with prompt recovery, even though two of these patients continued buprenorphine by the sublingual route. A fifth patient carrying the hepatitis C and human immunodeficiency viruses, developed jaundice and asterixis with panlobular liver necrosis and microvesicular steatosis after using sublingual buprenorphine and small doses of paracetamol and aspirin.

CONCLUSIONS Although buprenorphine hepatitis is most uncommon even after intravenous misuse, addicts placed on buprenorphine substitution should be repeatedly warned not to use it intravenously. Higher drug concentrations could trigger hepatitis in a few intravenous users, possibly those whose mitochondrial function is already impaired by viral infections and other factors

INTRODUCTION The use of ecstasy (MDMA) has developed in the young since the eighties. Among the severe adverse events induced by this synthetic drug, the hepatotoxicity related to MDMA and to its physiopathological mechanism warrant attention.

OBSERVATION A 21 year-old man consulted for anaemia that had persisted over the past months with abnormality in hepatic profile. The imputability of ecstasy in perturbations in his hepatic profile was highly probable in view of the fact that his transaminase level returned to normal one month after he stopped taking the drug, all the viral markers of hepatitis became negative and in the absence of concomitant consumption of any psycho-active drugs other than cannabis.

DISCUSSION A review of the literature showed the great variability in clinical pictures related to the hepato-toxicity of ecstasy, ranging from acute to lethal, fulminating hepatitis. The physiopathological mechanism of this phenomenon is little known. Various hypotheses are evoked with, among others, immuno-allergic-type hypersensitivity, phenomenon of apoptosis, vitamin E deficiency, and the role of occasionally concomitant malignant hyperthermia. The part played by the metabolites of the synthetic drug has also been suggested as well as individual variations in genetic origin with regards to the risk of developing acute hepatitis after ingestion of ecstasy.

The hepato-toxicity of this drug does not appear to be dose-dependant nor related to the cumulated duration of exposure

Traditional Chinese herbal medicines are widely available in Western society and are popular as a form of 'natural' alternative medicine. Their use is increasing, as they are perceived to be free of side effects, but they remain largely unregulated. We describe two patients who suffered severe hepatitis, one of whom died, after taking Chinese herbal remedies for minor complaints. We also review the English-language literature on hepatitis associated with Chinese herbs. Two products appear to be implicated frequently Jin bu huan was taken by 11 patients, and Dictamnus dasycarpus was taken by six patients, including both fatal cases. It is difficult to provide conclusive evidence of what caused hepatitis, as these products are mixtures that may contain adulterants. These cases highlight not only the potential dangers of these products to consumers but also the need for greater control of their manufacture and use.

AIMS Injection drug use is a major risk factor for HIV and hepatitis infections. Whereas programs to prevent new infections have focused on HIV, they have generally neglected hepatitis B and C. This study was designed to examine the interrelationships among HIV and hepatitis knowledge, risky drug preparation and injection practices, and participation in syringe exchange programs (SEPs).

PARTICIPANTS The study population was a convenience sample of 493 IDUs recruited using street outreach and snowball sampling strategies

FINDINGS HIV knowledge was significantly higher than hepatitis knowledge among SEP customers and non-customers alike. Elevated hepatitis knowledge was associated with a history of substance abuse treatment, hepatitis infection, hepatitis B vaccination and injection practices that reduced contact with contaminated blood or water but not with SEP use. SEP customers were consistently less likely to engage in risk behaviors, with the notable exception of safely staunching blood postinjection.

CONCLUSION Increased hepatitis awareness among IDUs is necessary for reducing hepatitis transmissions. Although SEPs continue to effectively disseminate HIV prevention messages-as evidenced by lowered risk behaviors among their customers-they must do more to prevent hepatitis transmissions.

OBJECTIVE To test the validity of drug users self-reports of diseases associated with drug use, in this case hepatitis A, B, and C.

DESIGN Injecting drug users (n 653) were recruited and asked whether they had been diagnosed previously with hepatitis A, B, and/or C. These self-report data were compared to total hepatitis A antibody, hepatitis B core antibody, and hepatitis C antibody seromarkers as a means of determining the validity of the self-reported information.

SETTING Anchorage, Alaska.

PARTICIPANTS Criteria for inclusion included being at least 18-years old testing positive on urinalysis for cocaine metabolites, amphetamine, or morphine having visible signs of injection (track marks).

INTRODUCTION We examined correlates of HBV infection and vaccination and the missed vaccination opportunities among young injection drug users (IDUs) and non-injection drug users (NIDUs).

METHODS Two hundred IDUs and 124 NIDUs aged 15-30 years were studied.

RESULTS More IDUs had been infected with HBV in the past than NIDUs (37 versus 19, P 0.001). Among male and female IDUs, injection drug use behaviors were significantly associated with past infection. For female IDUs, being African-American and trading sex were also associated with previous infection. Among NIDUs, being female and longer time since sexual debut were associated with past infection. Overall, 11 were vaccinated (10 IDU versus 14 NIDU, P 0.30). Younger age and drug treatment history were associated with vaccination. Most susceptibles (84) experienced at least one missed opportunity for vaccination.

CONCLUSION Young drug users remain at high risk for HBV infection. Vaccination rates remain low despite multiple opportunities for vaccination. An integrated HBV immunization effort should be coordinated among venues frequented by young drug users.

95SPECIAL CONSIDERATIONS

Chemically Dependent Patients

An outbreak of hepatitis A amongst injecting drug users. O'Donovan D

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For a small fee you can get the industry's best online privacy or publicly promote your presentations and slide shows with top rankings. But aside from that it's free. We'll even convert your presentations and slide shows into the universal Flash format with all their original multimedia glory, including animation, 2D and 3D transition effects, embedded music or other audio, or even video embedded in slides. All for free. Most of the presentations and slideshows on PowerShow.com are free to view, many are even free to download. (You can choose whether to allow people to download your original PowerPoint presentations and photo slideshows for a fee or free or not at all.) Check out PowerShow.com today - for FREE. There is truly something for everyone!